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Roland D. Thijs, Robert H.A. Reijntjes, J. Gert van Dijk
Department of Neurology and Clinical Neurophysiology, Leiden, The Netherlands

A 20-year-old male pupil of a sporting school had had attacks of lightheadedness over several months. The first time he felt unsteady and fell to the ground when he dismounted his bicycle after 1-hour of moderate exercise. In addition, he had chest pain and was short of breath. He was not certain whether or not he had passed out. Nobody had witnessed the event. For two hours afterwards he complained of unclear vision as if “looking through salad oil”. He had not been incontinent, had sustained no bruises and no tongue bite. Later, similar attacks occurred during light cycling, after competition skating, after skiing and during miction after exercise. He has a medical history of asthma and migraine. Both a cardiologist and a pulmonologist had analyzed the presenting complaints previously but could not find an explanation. Previous examinations had consisted of an ECG, echocardiography, bicycle stress testing, laboratory screen, chest X-ray and a lung perfusion scintigraphy. His medications were formoterol inhalations 12 mcg bid, budesonide inhalations 200 mcg bid and pantazol 20 mg od. The patient did not use coffee, nicotine or drugs. On physical examination no abnormalities were noted. The patient’s supine blood pressure (BP) was 110/65 mmHg with a resting heart rate (HR) of 70 beats per minute (bpm). Neurological examination showed slightly impaired fine motor skills and frequent eye blinks either left or right sided.

Treatment

A magnetic resonance imaging study of the brain was normal. Test of HR and BP during rest (70 bpm; 108/65 mmHg), deep breathing, standing up (85 bpm; 121/91 mmHg),a Valsalva maneuver and sustained hand grip were all normal. A tilt-table test (without medication) showed no abnormalities. Cathecholamine concentrations in plasma were obtained by venapuncture in both supine and after 30 minutes upright position (norepinephrine(NE): 1.22 nmol/l vs. 3.67 nmol/l, epinephrine(E): 0.13 vs. 0.16 nmol/l, dopamine(DA): 0.04 vs. 0.07 nmol/l, respectively) and in 24-hour urine (NE: 0.43 µmol, E: 0.06 µmol, DA: 2.46 µmol). In view of the relation to exercise, the patient was asked to mimic a typical bicycle tour on an ergometer, while EEG, ECG and BP (Finapres, finger photoplethysmography) were continuously monitored. Cycling at maximal effort increased HR up to 185 bpm (mean ± standard deviation: 176 ± 7 bpm) without significant BP changes (systolic BP (SBP) 119 ±14mmHg; diastolic BP (DBP) 72 ±9 mmHg). Immediately after cessation of exercise BP fell to 75/45 mmHg, during which the patient felt unsteady and complained of blurred vision; there was no loss of consciousness. During the BP drop, electrocardiography revealed sinus tachycardia of 180 bpm. The patient recognized the sensations as similar to those of spontaneous attacks. A second exercise test was performed two weeks later, 15 minutes after rapid consumption of 1000 mL water. Symptoms did not recur at the second test. Compared to the first cycling test the maximal rise of HR during exercise was reduced to 155 bpm and the BP raised during exercise (SBP 149 ± 21 mmHg; DBP 94 ± 14 mmHg). No significant BP drop occurred after cycling. Fig. 1 displays the changes of heart rate and blood pressure during both tests. Furthermore exercise-related symptoms were succesfully prevented by water ingestion. However, after 2 months our patient complained of attacks during ordinary daily activity. As these attacks could not be anticipated and occurred frequently, we advised to stop the extra water ingestion and precribed sodium tablets (7.2 g/day) instead. After 2 months he had had no complaints.

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